Reduction of bacterial load with the addition of ultraviolet-C disinfection inside the hyperbaric chamber.

INTRODUCTION: Healthcare acquired infections (HAIs) are associated with increased mortality, morbidity and prolonged hospital stays. Microbiological contamination of the hospital environment directly contributes to HAIs. Optimising environmental cleaning reduces transmission of HAIs. The hyperbaric chamber poses a specific challenge for infection control as certain disinfectants and alcohol-based hand sanitisers are prohibited due to fire risk. Patients often possess multiple risk factors for HAIs. This study compared the bacteria remaining on a surface (bioburden) after a standard clean and after adjunctive disinfection with an ultraviolet-C (UV-C) robot. METHODS: Internal hyperbaric chamber surfaces were first manually cleaned with Clinell® universal wipes and the floor was mopped with Whiteley neutral detergent. Allocated surfaces were swabbed using sterile cotton swabs and processed using a standard microbial culture and a bacteria-specific rapid metabolic assay. Bacterial contamination was also measured by direct contact plating on flat surfaces. The plexiglass ports were covered to protect from potential UV-C mediated damage and used as a negative control. A UV-C disinfection robot was then used to disinfect the chamber for 30 min, whereafter surfaces were swabbed again. RESULTS: There was a significantly greater mean reduction in bioburden following adjunctive UV-C disinfection than with standard cleaning alone. The surfaces not routinely manually cleaned (e.g., bench, phone) showed greatest reduction in bacterial load following UV-C cleaning. CONCLUSIONS: There was a significant reduction in the bacterial load in the chamber following an adjunctive UV-C clean compared with that of a standard clean. Adjunctive cleaning of the hyperbaric chamber environment with a non-touch UV-C device shows promise as a method to reduce HAIs.

Hyperbaric oxygen therapy for acute coronary syndrome.

BACKGROUND: Acute coronary syndrome (ACS), includes acute myocardial infarction and unstable angina, is common and may prove fatal. Hyperbaric oxygen therapy (HBOT) will improve oxygen supply to the threatened heart and may reduce the volume of heart muscle that perishes. The addition of HBOT to standard treatment may reduce death rate and other major adverse outcomes.This an update of a review previously published in May 2004 and June 2010. OBJECTIVES: The aim of this review was to assess the evidence for the effects of adjunctive HBOT in the treatment of ACS. We compared treatment regimens including adjunctive HBOT against similar regimens excluding HBOT. Where regimens differed significantly between studies this is clearly stated and the implications discussed. All comparisons were made using an intention to treat analysis where this was possible. Efficacy was estimated from randomised trial comparisons but no attempt was made to evaluate the likely effectiveness that might be achieved in routine clinical practice. Specifically, we addressed:Does the adjunctive administration of HBOT to people with acute coronary syndrome (unstable angina or infarction) result in a reduction in the risk of death?Does the adjunctive administration of HBOT to people with acute coronary syndrome result in a reduction in the risk of major adverse cardiac events (MACE), that is: cardiac death, myocardial infarction, and target vessel revascularization by operative or percutaneous intervention?Is the administration of HBOT safe in both the short and long term? SEARCH METHODS: We updated the search of the following sources in September 2014, but found no additional relevant citations since the previous search in June 2010 (CENTRAL), MEDLINE, EMBASE, CINAHL and DORCTHIM. Relevant journals were handsearched and researchers in the field contacted. We applied no language restrictions. SELECTION CRITERIA: Randomised studies comparing the effect on ACS of regimens that include HBOT with those that exclude HBOT. DATA COLLECTION AND ANALYSIS: Three authors independently evaluated the quality of trials using the guidelines of the Cochrane Handbook and extracted data from included trials. Binary outcomes were analysed using risk ratios (RR) and continuous outcomes using the mean difference (MD) and both are presented with 95% confidence intervals. We assessed the quality of the evidence using the GRADE approach. MAIN RESULTS: No new trials were located in our most recent search in September 2014. Six trials with 665 participants contributed to this review. These trials were small and subject to potential bias. Only two reported randomisation procedures in detail and in only one trial was allocation concealed. While only modest numbers of participants were lost to follow-up, in general there is little information on the longer-term outcome for participants. Patients with acute coronary syndrome allocated to HBOT were associated with a reduction in the risk of death by around 42% (RR: 0.58, (95% CI 0.36 to 0.92), 5 trials, 614 participants; low quality evidence).In general, HBOT was well-tolerated. No patients were reported as suffering neurological oxygen toxicity and only a single patient was reported to have significant barotrauma to the tympanic membrane. One trial suggested a significant incidence of claustrophobia in single occupancy chambers of 15% (RR of claustrophobia with HBOT 31.6, 95% CI 1.92 to 521). AUTHORS' CONCLUSIONS: For people with ACS, there is some evidence from small trials to suggest that HBOT is associated with a reduction in the risk of death, the volume of damaged muscle, the risk of MACE and time to relief from ischaemic pain. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT. The routine application of HBOT to these patients cannot be justified from this review.

Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus.

BACKGROUND: This is an update of a Cochrane Review first published in The Cochrane Library in Issue 1, 2005 and previously updated in 2007 and 2009.Idiopathic sudden sensorineural hearing loss (ISSHL) is common and has a significant effect on quality of life. Hyperbaric oxygen therapy (HBOT) may improve oxygen supply to the inner ear and result in an improvement in hearing. OBJECTIVES: To assess the benefits and harms of HBOT for treating ISSHL and/or tinnitus. SEARCH METHODS: We searched the Cochrane Ear, Nose and Throat Disorders Group Trials Register; the Cochrane Central Register of Controlled Trials (CENTRAL); PubMed; EMBASE; Database of Randomised Trials in Hyperbaric Medicine (DORCTHIM); CINAHL; Web of Science; BIOSIS Previews; Cambridge Scientific Abstracts; ICTRP and additional sources for published and unpublished trials. The date of the most recent search was 2 May 2012, following previous searches in 2009, 2007 and 2004. SELECTION CRITERIA: Randomised studies comparing the effect on ISSHL and tinnitus of HBOT and alternative therapies. DATA COLLECTION AND ANALYSIS: Three authors evaluated the quality of trials using the 'Risk of bias' tool and extracted data from the included trials. MAIN RESULTS: Seven trials contributed to this review (392 participants). The studies were small and of generally poor quality. Pooled data from two trials did not show any significant improvement in the chance of a 50% increase in hearing threshold on pure-tone average with HBOT (risk ratio (RR) with HBOT 1.53, 95% confidence interval (CI) 0.85 to 2.78, P = 0.16), but did show a significantly increased chance of a 25% increase in pure-tone average (RR 1.39, 95% CI 1.05 to 1.84, P = 0.02). There was a 22% greater chance of improvement with HBOT, and the number needed to treat (NNT) to achieve one extra good outcome was 5 (95% CI 3 to 20). There was also an absolute improvement in average pure-tone audiometric threshold following HBOT (mean difference (MD) 15.6 dB greater with HBOT, 95% CI 1.5 to 29.8, P = 0.03). The significance of any improvement in tinnitus could not be assessed.There were no significant improvements in hearing or tinnitus reported for chronic presentation (six months) of ISSHL and/or tinnitus. AUTHORS' CONCLUSIONS: For people with acute ISSHL, the application of HBOT significantly improved hearing, but the clinical significance remains unclear. We could not assess the effect of HBOT on tinnitus by pooled analysis. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously. An appropriately powered trial is justified to define those patients (if any) who can be expected to derive most benefit from HBOT.There is no evidence of a beneficial effect of HBOT on chronic ISSHL or tinnitus and we do not recommend the use of HBOT for this purpose.

Recompression and adjunctive therapy for decompression illness.

BACKGROUND: Decompression illness (DCI) is due to bubble formation in the blood or tissues following the breathing of compressed gas. Clinically, DCI may range from a trivial illness to loss of consciousness, death or paralysis. Recompression is the universally accepted standard treatment of DCI. When recompression is delayed, a number of strategies have been suggested in order to improve the outcome. OBJECTIVES: To examine the effectiveness and safety of both recompression and adjunctive therapies in the treatment of DCI. SEARCH METHODS: In our previous update we searched until October 2009. In this version we searched CENTRAL (The Cochrane Library, October 2011); MEDLINE (1966 to October 2011); CINAHL (1982 to October 2011); EMBASE (1980 to October 2011); the Database of Randomised Controlled Trials in Hyperbaric Medicine (October 2011); and handsearched journals and texts. SELECTION CRITERIA: We included randomized controlled trials that compared the effect of any recompression schedule or adjunctive therapy with a standard recompression schedule. We did not apply language restrictions. DATA COLLECTION AND ANALYSIS: Three authors extracted the data independently. We assessed each trial for internal validity and resolved differences by discussion. Data were entered into RevMan 5.1. MAIN RESULTS: Two randomized controlled trials enrolling a total of 268 patients satisfied the inclusion criteria. The risk of bias for Drewry 1994 was unclear as this study was presented as an abstract, while Bennett 2003 was rated as at low risk. Pooling of data was not possible. In one study there was no evidence of improved effectiveness with the addition of a non-steroidal anti-inflammatory drug (tenoxicam) to routine recompression therapy (at six weeks: relative risk (RR) 1.04, 95% confidence interval (CI) 0.90 to 1.20, P = 0.58) but there was a reduction in the number of compressions required when tenoxicam was added from three to two (P = 0.01, 95% CI 0 to 1). In the other study, the odds of multiple recompressions were lower with a helium and oxygen (heliox) table compared to an oxygen treatment table (RR 0.56, 95% CI 0.31 to 1.00, P = 0.05). AUTHORS' CONCLUSIONS: Recompression therapy is standard for the treatment of DCI, but there is no randomized controlled trial evidence for its use. Both the addition of a non-steroidal anti-inflammatory drug (NSAID) and the use of heliox may reduce the number of recompressions required, but neither improve the odds of recovery. The application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation. Benefits may be largely economic and an economic analysis should be undertaken. There is a case for large randomized trials of high methodological rigour in order to define any benefit from the use of different breathing gases and pressure profiles during recompression therapy.

Hyperbaric oxygen therapy for acute coronary syndrome.

BACKGROUND: Acute coronary syndrome (ACS), includes acute myocardial infarction and unstable angina, is common and may prove fatal. Hyperbaric oxygen therapy (HBOT) will improve oxygen supply to the threatened heart and may reduce the volume of heart muscle that perishes. The addition of HBOT to standard treatment may reduce death rate and other major adverse outcomes. OBJECTIVES: To assess the benefits and harms of adjunctive HBOT for treating ACS. SEARCH STRATEGY: We updated the search of the following sources in June 2010, finding one further trial: the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL, DORCTHIM, LILACS and checked the references from selected articles. Relevant journals were handsearched and researchers in the field contacted. No language restrictions were applied. SELECTION CRITERIA: Randomised studies comparing the effect on ACS of regimens that include HBOT with those that exclude HBOT. DATA COLLECTION AND ANALYSIS: Three reviewers independently evaluated the quality of trials using the guidelines of the Cochrane Handbook and extracted data from included trials. MAIN RESULTS: Six trials with 665 participants contributed to this review. There was a significant decrease in the risk of death with HBOT (risk ratio (RR) 0.58, 95% CI 0.36 to 0.92, P = 0.02). The extent of heart muscle damage was lower following HBOT, as shown by a lesser rise in muscle enzyme in the blood (mean difference (MD) 493 IU, P = 0.005) and a better LVEF (MD 5.5%, P = 0.001). There was evidence from individual trials of reductions in the risk of major adverse coronary events (MACE) (RR 0.12, P = 0.03); re-infarction (RR 0.28, P = 0.04) and dysrhythmias following HBOT (RR 0.59, P = 0.01, and the time to relief of pain was reduced with HBOT (MD 353 minutes shorter, P < 0.00001). One trial suggested a significant incidence of claustrophobia in single occupancy chambers of 15% (RR of claustrophobia with HBOT 31.6, P = 0.02). AUTHORS' CONCLUSIONS: For people with ACS, there is some evidence from small trials to suggest that HBOT is associated with a reduction in the risk of death, the volume of damaged muscle, the risk of MACE and time to relief from ischaemic pain. In view of the modest number of patients, methodological shortcomings and poor reporting, this result should be interpreted cautiously, and an appropriately powered trial of high methodological rigour is justified to define those patients (if any) who can be expected to derive most benefit from HBOT. The routine application of HBOT to these patients cannot be justified from this review.

Recompression and adjunctive therapy for decompression illness: a systematic review of randomized controlled trials.

INTRODUCTION: Decompression illness (DCI) is caused by bubble formation in the blood or tissues after a reduction in ambient pressure. Clinically, DCI may range from a trivial illness to paralysis, loss of consciousness, cardiovascular collapse, and death. Recompression is the universally accepted standard for the treatment of DCI. When recompression is delayed, a number of strategies have been suggested to improve the outcome. We examined the effectiveness and safety of both recompression and adjunctive therapies in the treatment of DCI. METHODS: We searched CENTRAL (Cochrane Central Register of Controlled Trials) (The Cochrane Library 2009, Issue 2); MEDLINE (Medical Literature Analysis and Retrieval System Online) (1966 to July 2009); CINAHL (Cumulative Index to Nursing and Allied Health Literature) (1982 to July 2009); EMBASE (Excerpta Medica Database) (1980 to July 2009); the Database of Randomized Controlled Trials (RCTs) in Hyperbaric Medicine (July 2009); and hand-searched journals and texts. We included RCTs that compared the effect of any recompression schedule or adjunctive therapy with a standard recompression schedule and applied no language restrictions. Three authors extracted the data independently. We assessed each trial for internal validity and resolved differences by discussion. Data were entered into RevMan 5.0 software (Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2008). RESULTS: Two RCTs satisfied the inclusion criteria. Pooling of data was not possible. In one study, there was no evidence of improved effectiveness with the addition of a nonsteroidal antiinflammatory drug to routine recompression therapy (at 6 weeks: relative risk 1.04, 95% confidence interval [CI]: 0.90-1.20, P = 0.58), but there was a reduction in the number of recompression treatments required when tenoxicam was added (P = 0.01, 95% CI: 0-1). In the other study, the odds of multiple recompressions were lower with a helium and oxygen (heliox) table compared with an oxygen treatment table (relative risk 0.56, 95% CI: 0.31-1.00, P = 0.05). DISCUSSION: Recompression therapy is the standard for treatment of DCI, but there is no RCT evidence. The addition of a nonsteroidal antiinflammatory drug (tenoxicam) or the use of heliox may reduce the number of recompressions required, but neither improves the odds of recovery. The application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation. Benefits may be largely economic, and an economic analysis should be undertaken. There is a case for large randomized trials of high methodological rigor to define any benefit from the use of different breathing gases and pressure profiles during recompression.

Recompression and adjunctive therapy for decompression illness: a systematic review of randomised controlled trials.

INTRODUCTION: Decompression illness (DCI) results from bubble formation in the blood or tissues following the breathing of compressed gas. Recompression is the universally accepted standard for the treatment of DCI, but a number of strategies have been suggested in order to improve the outcome. METHODS: We performed a systematic search of the literature in December 2007 for randomised controlled trials of DCI therapy, and made an analysis of pre-determined clinical outcomes. RESULTS: Two randomised controlled trials satisfied the inclusion criteria. Pooling of data was not possible. There was a reduction in the number of compressions required with the addition of the non-steroidal anti-inflammatory drug (NSAID) tenoxicam to routine recompression therapy (P = 0.01) but no evidence of improved effectiveness (relative risk (RR) of residual symptoms 1.04, P = 0.58). The risk of multiple recompressions was lower with heliox than with an oxygen treatment table (RR 0.56, 95% CI 0.31 to 1.00, P = 0.05). CONCLUSIONS: There is no randomised evidence concerning the effectiveness of recompression for DCI. Either the addition of an NSAID or the use of heliox may reduce the number of recompressions required, but neither strategy is shown to improve the chance of recovery. The application of either of these strategies may be justified. The modest number of patients studied demands a cautious interpretation of the findings. There is a case for large randomised trials of high methodological rigour in order to define any benefit from the use of different breathing gases during recompression therapy.